Abstract：
Permethrin (Per) is a widely used and frequently detected pyrethroid pesticide in agricultural products and the environment. It may pose potential toxicity to non-target organisms. Per has been reported to affect lipid homeostasis, although the mechanism is undefined. This study aims to explore the characteristic transcriptomic profiles and clarify the underlying signaling pathways of Per-induced lipid metabolism disorder in zebrafish liver. The results showed that environmental exposure to Per caused changes in the liver index, histopathology, and oxidative stress in zebrafish. Moreover, transcriptome results showed that Per heavily altered the pathways involved in metabolism, the immune system, and the endocrine system. We conducted a more in-depth analysis of the genes associated with lipid metabolism. Our findings revealed that exposure to Per led to a disruption in lipid metabolism by activating the KRAS-PPAR-GLUT signaling pathways through oxidative stress. The disruption of lipid homeostasis caused by exposure to Per may also contribute to obesity, hepatitis, and other diseases. The results may provide new insights for the risk of Permethrin to aquatic organisms and new horizons for the pathogenesis of hepatotoxicity.
摘要：
氯菊酯（Per）是一种广泛使用且在农产品和环境中经常检测到的拟除虫菊酯农药。它可能对非靶标生物造成潜在毒性。据报道，Per会影响脂质稳态，尽管机制未定义。本研究旨在探索斑马鱼肝脏中Per诱导脂质代谢紊乱的特征性转录组学谱并阐明其潜在的信号通路。结果表明，环境暴露于Per引起肝脏指数的变化，组织病理学,和斑马鱼的氧化应激。此外，转录组结果显示，Per严重改变了参与代谢的途径，免疫系统,和内分泌系统。我们对与脂质代谢相关的基因进行了更深入的分析。我们的发现表明，暴露于Per通过氧化应激激活KRAS-PPAR-GLUT信号通路导致脂质代谢中断。暴露于Per引起的脂质稳态的破坏也可能导致肥胖，肝炎，和其他疾病。该结果可能为氯菊酯对水生生物的风险提供新的见解，并为肝毒性的发病机理提供新的视野。
